Project Summary/Abstract Children with all levels of sleep-disordered breathing (SDB) are at increased risk for deficits in executive function, leading to impairments in behavior regulation and reduced academic achievement. The mechanisms linking SDB to daytime deficits are thought to include sleep disruption and/or neural damage from hypoxemia, but the relative contribution of each is unclear. Analyses of slow-wave activity (SWA) in non-rapid eye movement (NREM) sleep, a marker of both the restorative function of sleep and neural plasticity, have failed to consistently identify differences between SDB and healthy controls. The reasons for the inconsistencies in these data are likely multifactorial, but recent theoretical and technological advances highlight two likely contributors. First, our conceptual understanding of sleep has changed dramatically in the past few years; we now know that sleep is not a global, whole brain phenomenon, but instead is a process that can, and does, occur regionally. Regional sleep is particularly relevant during development; recent data demonstrate that the peak distribution of cortical SWA changes as a function of age. Prior EEG investigations of sleep in SDB have used standard clinical EEG montages that use only a few scalp electrodes. Given the developmental trajectory of SWA, such limited montages are not optimized to capture the distribution of SWA in the developing brain. Second, we now know that sleep and wake can co-exist in the brain. Recent data demonstrates that when neurons get `sleepy' due to extended use or sleep deprivation, they account for this by going to sleep, interrupting and resuming their discharge pattern as they do in sleep, in an otherwise wake brain. Critically, when neurons go to sleep in areas relevant for behavior, the result in lapses in neurobehavioral performance. Using high-density EEG (hdEEG, 256 channel electroencephalography) we recently identified a reduction in SWA in the posterior cortex during NREM in a group of 5-13 year old children with SDB suggesting the presence of local impairments in sleep restoration and quality. Our central hypothesis is that regional loss of nocturnal SWA will result in episodes of local sleep during wakefulness that will underpin the well-documented daytime impairments common to SBD. We will test our hypothesis by 1. Confirming regional reductions in SWA in a larger group of children with SDB, and 2. Examining the relationship between neurobehavioral lapses and daytime theta activity (an EEG index of local sleep). The proposed study will increase our understanding of mechanisms contributing to daytime impairment in pediatric SDB as well as provide pilot data to design a future study to assess the effect of treatment on sleep EEG and daytime function.